Colloids decrease clot propagation and strength: role of factor XIII-fibrin polymer and thrombin-fibrinogen...

Area of Science:

• Biochemistry
• Hematology
• Physiology

Background:

• Colloid administration is common in clinical settings.
• Colloid-mediated hypocoagulability (reduced blood clotting) is a known complication.
• The precise mechanisms behind this coagulopathy are not fully understood.

Purpose of the Study:

• To investigate how different colloids, including hydroxyethyl starches (HES) and albumin, affect plasma coagulation.
• To elucidate the specific molecular mechanisms responsible for colloid-induced impairment of blood clot formation.
• To identify potential therapeutic targets for counteracting colloid-related bleeding risks.

Main Methods:

• Plasma samples were diluted with saline, various HES solutions, or albumin.
• Diluted samples were supplemented with fibrinogen (FI), thrombin (FIIa), or activated Factor XIII (FXIIIa).
• Thrombelastography was used to measure clot propagation and strength, assessing the impact of colloids and supplements.

Main Results:

• Dilution with NaCl, HES, and albumin significantly reduced clot propagation and strength.
• Fibrinogen supplementation normalized clotting in NaCl-diluted plasma but only partially in colloid-diluted plasma.
• Thrombin and Factor XIIIa supplementation showed varied, partial improvements in clot parameters depending on the colloid used.

Conclusions:

• Colloids compromise plasma coagulation primarily by interfering with Factor IIa-fibrinogen and Factor XIIIa-fibrin polymer interactions.
• Partial restoration of coagulation was observed with fibrinogen and Factor XIIIa supplementation.
• Further clinical investigation into enhancing Factor XIII activity and fibrinogen levels is warranted to manage colloid-induced hypocoagulability.